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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Supraspinal delta 2 opioid agonist analgesia in Swiss-Webster mice involves spinal GABAA receptors.
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Supraspinal delta 2 opioid agonist analgesia in Swiss-Webster mice involves spinal GABAA receptors.

机译：Swiss-Webster小鼠的Suspaspinal delta 2阿片样物质激动剂镇痛涉及脊髓GABAA受体。

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The tail-flick response is a spinal reflex that can be modulated by administration of antinociceptive agents supraspinally through activation of descending systems and involvement of the action of neurotransmitters in the spinal cord. Descending noradrenergic and serotonergic systems are involved in morphine (and other mu opioid receptor agonists)-induced antinociception. These descending systems, however, are not involved in supraspinal delta opioid receptor agonist-induced antinociception. Recently, a descending system mediated by spinal gamma-aminobutyric acid (GABA) A and B receptors has been demonstrated to be involved in the antinociceptive action of delta 1 opioid receptor agonists ([D-Pen2,5]enkephalin in ICR mice and [D-Pen2,5]enkephalin and heroin in Swiss-Webster mice). In the present study, the involvement of spinal GABAA receptors in the antinociceptive action of supraspinal delta 2 opioid receptor agonists, [D-Ser2]-Leu-enkephalin-Thr and 6-monoacetylmorphine, action was demonstrated. Theintrathecal administration of GABAA receptor antagonists, bicuculline and picrotoxin, inhibited the antinociceptive action of both [D-Ser2]-Leu-enkephalin-Thr and 6-monoacetylmorphine given intracerebroventricularly. The intrathecal administration of 2-hydroxysaclofen, a GABAB receptor antagonist, had no effect. These studies suggest that supraspinal delta 2, like delta 1, opioid receptor action involves spinal GABAA receptors, but delta 2, unlike delta 1, action does not involve GABAB receptors. Thus, the supraspinal delta 1 agonist action (heroin, DPDPE) and the delta 2 agonist action (6MAM, DSLET) can be further differentiated by the selectivity of the spinal GABA receptors involved in Swiss-Webster mice.
机译：甩尾反应是一种脊柱反射，可通过降系的激活和神经递质在脊髓中的参与，通过向脊髓上施用抗伤害感受药来调节。去甲肾上腺素能和5-羟色胺能系统参与吗啡（和其他μ阿片受体激动剂）诱导的镇痛作用。然而，这些下降系统不参与脊髓上三角洲阿片样物质受体激动剂诱导的抗伤害感受。最近，已证明由脊髓γ-氨基丁酸（GABA）A和B受体介导的递减系统参与了ICR小鼠和[D]中的delta 1阿片类受体激动剂（[D-Pen2,5]脑啡肽的镇痛作用）。 -Pen2,5]脑啡肽和海洛因在Swiss-Webster小鼠中）。在本研究中，表明了脊髓GABAA受体参与了脊髓上三角洲2阿片样物质受体激动剂[D-Ser2] -Leu-脑啡肽-Thr和6-单乙酰吗啡的镇痛作用。鞘内给予GABAA受体拮抗剂，双小分子和苦瓜毒素，可抑制脑室内给予[D-Ser2] -Leu-脑啡肽-Thr和6-单乙酰吗啡的镇痛作用。鞘内注射GABAB受体拮抗剂2-羟基沙氯芬无效。这些研究表明，脊髓上三角洲2，像三角洲1，阿片受体的作用涉及脊髓GABAA受体，但三角洲2，不同于三角洲1，作用不涉及GABA B受体。因此，可以通过参与Swiss-Webster小鼠的脊髓GABA受体的选择性进一步区分上棘上δ1激动剂作用（海洛因，DPDPE）和δ2激动剂作用（6MAM，DSLET）。

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